Stories from the Creativity Garden: A Series of Interviews with Dr. Mary Murdock

This project explores the curricular development of the Creativity Domain fromthe perspective of Dr. Mary Murdock in a series of informal discussions and video clips with me. We discuss some of the curriculum highlights and processes that she has worked with from her time as a graduate assistant in Georgia to her tenure at Buffalo State College. The recordings have been created in a documentary format as pod casts as Dr. Murdock discusses the domain of creativity, curriculum and methodology of the delivery of theory and the processes inherent. The intent has been to dig deeper into several key process areas (socio drama, Creative Problem Solving, Torrance Incubation Model, Thinking Skills Model) with the audio interview recordings reflecting the passion and highlights of Dr. Murdock’s pedagogical interests, pursuits and strengths. The final portion of the collection includes an audio interview and video excerpt on the TIM and a presentation of Dr. Murdock’s living creativity garden at her home, created by Dr. Susan Keller-Mathers. The focus of interest is on the academic curricular aspect and the organic nature of creativity and not the facilitative model

cMOOCs and Global Learning: An Authentic Alternative

Massive Open Online Courses (MOOCs) continue to attract press coverage as they change almost daily in their format, number of registrations and potential for credentialing. An enticing aspect of the MOOC is its global reach. In this paper, we will focus on a type of MOOC called a cMOOC, because it is based on the theory of connectivism and fits the definition of an Open Educational Resource (OER) identified for this special edition of JALN. We begin with a definition of the cMOOC and a discussion of the connectivism on which it is based. Definitions and a research review are followed with a description of two MOOCs offered by two of the authors. Research on one of these MOOCs completed by a third author is presented as well. Student comments that demonstrate the intercultural connections are shared. We end with reflections, lessons learned and recommendations

Investigating the Direct and Indirect Effects of Forest Fragmentation on Plant Functional Diversity

Ongoing habitat loss and fragmentation alter the functional diversity of forests. Generalising the magnitude of change in functional diversity of fragmented landscapes and its drivers is challenging because of the multiple scales at which landscape fragmentation takes place. Here we propose a multi-scale approach to determine whether fragmentation processes at the local and landscape scales are reducing functional diversity of trees in the East Usambara Mountains, Tanzania. We employ a structural equation modelling approach using five key plant traits (seed length, dispersal mode, shade tolerance, maximum tree height, and wood density) to better understand the functional responses of trees to fragmentation at multiple scales. Our results suggest both direct and indirect effects of forest fragmentation on tree functional richness, evenness and divergence. A reduction in fragment area appears to exacerbate the negative effects resulting from an increased amount of edge habitat and loss of shape complexity, further reducing richness and evenness of traits related to resource acquisition and favouring tree species with fast growth. As anthropogenic disturbances affect forests around the world, we advocate to include the direct and indirect effects of forest fragmentation processes to gain a better understanding of shifts in functional diversity that can inform future management efforts

How can we inspire nations of learners? Investigating growth mindset and challenge-seeking in two countries

© American Psychological Association, 2020. This paper is not the copy of record and may not exactly replicate the authoritative document published in the APA journal. Please do not copy or cite without author's permission. The final article is available, upon publication, at: https://doi.org/10.1037/amp0000647Here we evaluate the potential for growth mindset interventions (which teach students that intellectual abilities can be developed) to inspire adolescents to be “learners”—that is, to seek out challenging learning experiences. In a previous analysis, the U.S. National Study of Learning Mindsets (NSLM) showed that a growth mindset could improve the grades of lower-achieving adolescents, and, in an exploratory analysis, increase enrollment in advanced math courses across achievement levels. Yet the importance of being a “learner” in today’s global economy requires clarification and replication of potential challenge-seeking effects, as well as an investigation of the school affordances that make intervention effects on challenge-seeking possible. To this end, the present paper presents new analyses of the U.S. NSLM (N = 14,472) to (a) validate a standardized, behavioral measure of challenge-seeking (the “make-a-math worksheet” task), and (b) show that the growth mindset treatment increased challenge-seeking on this task. Second, a new experiment conducted with nearly all schools in two counties in Norway, the U-say experiment (N = 6,541), replicated the effects of the growth mindset intervention on the behavioral challenge-seeking task and on increased advanced math course-enrollment rates. Treated students took (and subsequently passed) advanced math at a higher rate. Critically, the U-say experiment provided the first direct evidence that a structural factor—school policies governing when and how students opt in to advanced math—can afford students the possibility of profiting from a growth mindset intervention or not. These results highlight the importance of motivational research that goes beyond grades or performance alone and focuses on challenge-seeking. The findings also call attention to the affordances of school contexts that interact with student motivation to promote better achievement and economic trajectories.acceptedVersio

Short Telomeres Initiate Telomere Recombination in Primary and Tumor Cells

Human tumors that lack telomerase maintain telomeres by alternative lengthening mechanisms. Tumors can also form in telomerase-deficient mice; however, the genetic mechanism responsible for tumor growth without telomerase is unknown. In yeast, several different recombination pathways maintain telomeres in the absence of telomerase—some result in telomere maintenance with minimal effects on telomere length. To examine non-telomerase mechanisms for telomere maintenance in mammalian cells, we used primary cells and lymphomas from telomerase-deficient mice (mTR−/− and Eμmyc+mTR−/−) and CAST/EiJ mouse embryonic fibroblast cells. These cells were analyzed using pq-ratio analysis, telomere length distribution outliers, CO-FISH, Q-FISH, and multicolor FISH to detect subtelomeric recombination. Telomere length was maintained during long-term growth in vivo and in vitro. Long telomeres, characteristic of human ALT cells, were not observed in either late passage or mTR−/− tumor cells; instead, we observed only minimal changes in telomere length. Telomere length variation and subtelomeric recombination were frequent in cells with short telomeres, indicating that length maintenance is due to telomeric recombination. We also detected telomere length changes in primary mTR−/− cells that had short telomeres. Using mouse mTR+/− and human hTERT+/− primary cells with short telomeres, we found frequent length changes indicative of recombination. We conclude that telomere maintenance by non-telomerase mechanisms, including recombination, occurs in primary cells and is initiated by short telomeres, even in the presence of telomerase. Most intriguing, our data indicate that some non-telomerase telomere maintenance mechanisms occur without a significant increase in telomere length

Genome-wide association study identifies multiple risk loci for renal cell carcinoma

Previous genome-wide association studies (GWAS) have identified six risk loci for renal cell carcinoma (RCC). We conducted a meta-analysis of two new scans of 5,198 cases and 7,331 controls together with four existing scans, totalling 10,784 cases and 20,406 controls of European ancestry. Twenty-four loci were tested in an additional 3,182 cases and 6,301 controls. We confirm the six known RCC risk loci and identify seven new loci at 1p32.3 (rs4381241, P=3.1 × 10−10), 3p22.1 (rs67311347, P=2.5 × 10−8), 3q26.2 (rs10936602, P=8.8 × 10−9), 8p21.3 (rs2241261, P=5.8 × 10−9), 10q24.33-q25.1 (rs11813268, P=3.9 × 10−8), 11q22.3 (rs74911261, P=2.1 × 10−10) and 14q24.2 (rs4903064, P=2.2 × 10−24). Expression quantitative trait analyses suggest plausible candidate genes at these regions that may contribute to RCC susceptibility

A genome-wide association study of marginal zone lymphoma shows association to the HLA region

Marginal zone lymphoma (MZL) is the third most common subtype of B-cell non-Hodgkin lymphoma. Here we perform a two-stage GWAS of 1,281 MZL cases and 7,127 controls of European ancestry and identify two independent loci near BTNL2 (rs9461741, P - 3.95 x 10(-15)) and HLA-B (rs2922994, P - 2.43 x 10(-9)) in the HLA region significantly associated with MZL risk. This is the first evidence that genetic variation in the major histocompatibility complex influences MZL susceptibility

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Sex specific associations in genome wide association analysis of renal cell carcinoma.

Renal cell carcinoma (RCC) has an undisputed genetic component and a stable 2:1 male to female sex ratio in its incidence across populations, suggesting possible sexual dimorphism in its genetic susceptibility. We conducted the first sex-specific genome-wide association analysis of RCC for men (3227 cases, 4916 controls) and women (1992 cases, 3095 controls) of European ancestry from two RCC genome-wide scans and replicated the top findings using an additional series of men (2261 cases, 5852 controls) and women (1399 cases, 1575 controls) from two independent cohorts of European origin. Our study confirmed sex-specific associations for two known RCC risk loci at 14q24.2 (DPF3) and 2p21(EPAS1). We also identified two additional suggestive male-specific loci at 6q24.3 (SAMD5, male odds ratio (ORmale) = 0.83 [95% CI = 0.78-0.89], Pmale = 1.71 × 10-8 compared with female odds ratio (ORfemale) = 0.98 [95% CI = 0.90-1.07], Pfemale = 0.68) and 12q23.3 (intergenic, ORmale = 0.75 [95% CI = 0.68-0.83], Pmale = 1.59 × 10-8 compared with ORfemale = 0.93 [95% CI = 0.82-1.06], Pfemale = 0.21) that attained genome-wide significance in the joint meta-analysis. Herein, we provide evidence of sex-specific associations in RCC genetic susceptibility and advocate the necessity of larger genetic and genomic studies to unravel the endogenous causes of sex bias in sexually dimorphic traits and diseases like RCC